Figure 8.

Effects of NOX4, CD44V6, and ROS on TGFβ1-induced HNLFb collagen matrix contractility. A, HNLFbs embedded in three-dimensional collagen matrices were treated with NOX4 shRNA, a NOX inhibitor, GKT137831 (1 μm (obtained from a dose-response experiment for NOX4 inhibition)), an endogenous CD44V6 competing peptide (V6-PEP), or a catalase expression vector (a ROS inhibitor) before treatment with TGFβ1 (2.5 ng/ml for 72 h) followed by measurements of matrix contractility (area of gel). Data represent mean ± S.E. (error bars); n = 3; *, p < 0.005 compared with untreated controls. B, representative Western blots are shown for expression of α-SMA and β-actin in lysates from cells transfected with control shRNA (cont) or NOX4 shRNA, or treated with 1 μm GKT137831, or transfected with catalase, or treated with control peptide (cont), or treated with CD44v6-blocking peptide (V6-PEP) for 24 h and then incubated with TGFβ1 (2.5 ng/ml for 72 h). The experimental data in A and B are from three sets of three independent experiments. Statistical analysis was with ANOVA; A, *, p ≤ 0.01 versus the respective control group.